scholarly journals Erratum: Erratum: Myc overexpression enhances epicardial contribution to the developing heart and promotes extensive expansion of the cardiomyocyte population

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Cristina Villa del Campo ◽  
Ghislaine Lioux ◽  
Rita Carmona ◽  
Rocío Sierra ◽  
Ramón Muñoz-Chápuli ◽  
...  
Keyword(s):  
Developing Heart ◽  
Cardiomyocyte Population

scholarly journals Regulation of the cardiomyocyte population in the developing heart

2011 ◽  
Vol 106 (1) ◽  
pp. 289-299 ◽  
Author(s):  
Kent Thornburg ◽  
Sonnet Jonker ◽  
Perrie O’Tierney ◽  
Natasha Chattergoon ◽  
Samantha Louey ◽  
...  
Keyword(s):  
Developing Heart ◽  
Cardiomyocyte Population

Subclinical Thyroid Dysfunction and the Risk of Cardiovascular Disease

2020 ◽  
Vol 26 (43) ◽  
pp. 5617-5627
Author(s):  
Mirjana Stojković ◽  
Miloš Žarković
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Cardiac Electrophysiology ◽  
Vascular System ◽  
Density Lipoprotein ◽  
Thyroid Stimulating Hormone ◽  
Normal Limits ◽  
Developing Heart ◽  
Treatment Indications ◽  
Increased Risk

The prevalence of subclinical hypothyroidism (SH) is 3-10%. The prevalence of subclinical hyperthyroidism (SHr) is 0.7-9.7%. Thyroid hormones affect cardiac electrophysiology, contractility, and vasculature. SH is associated with an increased risk of coronary heart disease (CHD), especially in subjects under 65. SHr seems to be associated with a slightly increased risk of CHD and an increase in CHD-related mortality. Both SH and SHr carry an increased risk of developing heart failure (HF), especially in those under 65. Both SH and SHr are associated with worse prognoses in patients with existing HF. SH is probably not associated with atrial fibrillation (AF). SHr, low normal thyroid-stimulating hormone (TSH) and high normal free thyroxine (FT4) are all associated with the increased risk of AF. An association between endothelial dysfunction and SH seems to exist. Data regarding the influence of SHr on the peripheral vascular system are conflicting. SH is a risk factor for stroke in subjects under 65. SHr does not increase the risk of stroke. Both SH and SHr have an unfavourable effect on cardiovascular disease (CVD) and all-cause mortality. There is a U-shaped curve of mortality in relation to TSH concentrations. A major factor that modifies the relation between subclinical thyroid disease (SCTD) and mortality is age. SH increases blood pressure (BP). SHr has no significant effect on BP. Lipids are increased in patients with SH. In SHr, high-density lipoprotein cholesterol and lipoprotein( a) are increased. SCTD should be treated when TSH is over 10 mU/l or under 0.1 mU/l. Treatment indications are less clear when TSH is between normal limits and 0.1 or 10 mU/L. The current state of knowledge supports the understanding of SCTD’s role as a risk factor for CVD development. Age is a significant confounding factor, probably due to age-associated changes in the TSH reference levels.

scholarly journals Clinical and echocardiographic trends in percutaneous balloon mitral valvuloplasty

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Ofir Koren ◽  
Asaf Israeli ◽  
Ehud Rozner ◽  
Nassem Darawshy ◽  
Yoav Turgeman
Keyword(s):  
Heart Failure ◽  
Medical Center ◽  
Success Rates ◽  
Mitral Valvuloplasty ◽  
Percutaneous Balloon Mitral Valvuloplasty ◽  
Developing Heart ◽  
Percutaneous Balloon ◽  
Study Population ◽  
Procedural Success ◽  
Over Time

Abstract Background The prevalence of Rheumatic Mitral Stenosis (MS) has significantly changed over the last decades. We intend to examine patient demographics, Echocardiographic characteristics, procedural success rates, and complications throughout 30-years. Methods We conducted a single-center descriptive observational study. The study population consists of patients undergone percutaneous balloon mitral valvuloplasty (PBMV) at Emek Medical Center in Israel from January 1990 to May 2019. Results Four hundred seventeen patients underwent PBMV during the study period and were eligible for the study. Age did not change significantly over time (p = 0.09). The prevalence of Male and patients who were smoking and had multiple comorbidities such as hypertension, dyslipidemia, ischemic heart disease, and chronic kidney disease became increases over time (p = 0.02, p = 0.02, p = 0.001, p = 0.01, p = 0.02, and p = 0.001, respectively). Wilkins score and all its components increased over time, and the total score was higher in females (p = 0.01). Seventy-nine (18.9%) patients had complications. The rate of complications did not change over decades. Patients with Wilkins score > 8, post-procedural MR of ≥2, and post-procedural MVA < 1.5 had the highest risk for the need of Mitral valve replacement (MVR) surgery in 2 years following PBMV (3.64, 4.03, 2.44, respectively, CI 95%, p < .0001 for all). The median time in these patients was 630 days compared to 4–5 years in the entire population. Patients with Post-procedural MR of ≥2 and post-procedural MVA < 1.5 had ten times risk for developing heart failure (HR 9.07 and 10.06, respectively, CI 95%, P < .0001). Conclusion Our research reveals trends over time in patients’ characteristics and echocardiographic features. Our study population consists of more male patients with multiple comorbidities and more complex and calcified valvular structures in the last decade. Wilkins score > 8, post-procedural MR of ≥2, and post-procedural MVA < 1.5 cm2 were in-depended predictors for the time for surgery and heart failure hospitalization.

The effect of oestrogen withdrawal on cardiac Ca2+ regulation and the influence of GPER1

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A.J Francis ◽  
J.M Firth ◽  
N Islam ◽  
J Gorelik ◽  
K.T MacLeod
Keyword(s):  
Heart Failure ◽  
Structural Integrity ◽  
Left Ventricular ◽  
Funding Source ◽  
Hormonal Changes ◽  
Ion Conductance ◽  
Developing Heart ◽  
Rapid Stimulation ◽  
Post Menopausal

Abstract Background Post-menopausal women have an enhanced risk of developing heart failure, attributed to declining oestrogen levels during menopause. However, the signalling mechanisms remain undetermined. Purpose We aim to determine the role of G-protein coupled oestrogenic receptor 1 (GPER1) in intracellular Ca2+ regulation and the consequences of hormonal changes that may exacerbate the pathophysiology of heart failure. Methods Ovariectomy (OVx) (mimics menopausal hormone changes) or sham surgeries were conducted on female guinea pigs. Left ventricular cardiomyocytes were isolated 150-days post-operatively for experimental use. Cellular t-tubule network and structural integrity was measured using fluorescent di-8-ANEPPs staining and scanning ion conductance microscopy. GPER1 expression and localisation was measured by Western blot and immunostaining. The role of GPER1 activation was measured using selective agonist G-1 in electrophysiological and Ca2+-sensitive dye fluorescence experiments. Results Following oestrogen withdrawal, the t-tubule network density decreased by 13% and z-groove index reduced by 15%. GPER1 predominantly localised to the peri-nuclear endoplasmic reticulum and its expression increased by 32% in OVx. Action potential duration (APD) prolonged in OVx and following GPER1 activation, APD90 shortened by 11% and 25% in sham and OVx respectively. OVx cells had larger peak inward Ca2+ current (ICaL) (by 22%) and sarcoplasmic reticulum (SR) Ca2+ content (by 13%), compared with sham. While GPER1 activation had little effect on peak ICaL or SR content, it reduced Ca2+ transient amplitude (by 20%), SR fractional release (by 11%) in OVx cells. The frequency of occurrence of spontaneous Ca2+ waves evoked by periods of rapid stimulation reduced by 40% and wave-free survival time prolonged in OVx cells following GPER1 activation. Conclusions In the hearts of an animal species whose electrophysiology and intracellular Ca2+ regulation is akin to humans, we show that following oestrogen deficiency, the t-tubule network is down-regulated and becomes disorganised, GPER1 expression is increased and its activation induces negative inotropic responses in cardiomyocytes. This may limit the adverse changes to Ca2+ signalling reported in OVx that could be pro-arrhythmic and exacerbate the progression to heart failure. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation

scholarly journals GATA-4/5/6, a subfamily of three transcription factors transcribed in developing heart and gut.

1994 ◽  
Vol 269 (37) ◽  
pp. 23177-23184 ◽  
Author(s):  
A.C. Laverriere ◽  
C. MacNeill ◽  
C. Mueller ◽  
R.E. Poelmann ◽  
J.B. Burch ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Developing Heart

Arrhythmias in the developing heart

2014 ◽  
Vol 213 (2) ◽  
pp. 303-320 ◽  
Author(s):  
D. Sedmera ◽  
R. Kockova ◽  
F. Vostarek ◽  
E. Raddatz
Keyword(s):  
Developing Heart

scholarly journals 4D shear stress maps of the developing heart using Doppler optical coherence tomography

2012 ◽  
Vol 3 (11) ◽  
pp. 3022 ◽  
Author(s):  
Lindsy M. Peterson ◽  
Michael W. Jenkins ◽  
Shi Gu ◽  
Lee Barwick ◽  
Michiko Watanabe ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Shear Stress ◽  
Optical Coherence ◽  
Developing Heart ◽  
Doppler Optical Coherence Tomography

Abstract 350: Atorvastatin Attenuates Pressure Overload-induced Cardiac Hypertrophy and Dysfunction Through Enhanced Autophagy

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Zhuo Zhao ◽  
Wei Wang ◽  
Hua-Ting Wang ◽  
Qing-Xin Geng ◽  
Di Zhao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Mrna Level ◽  
Mammalian Target Of Rapamycin ◽  
Pressure Overload ◽  
Oral Gavage ◽  
Atorvastatin Treatment ◽  
Developing Heart ◽  
Phosphorylated Akt

Aims: Cardiac hypertrophy is a maladaptive change in response to pressure overload and is also an important risk for developing heart failure. We previously demonstrated that atorvastatin inhibits cardiac hypertrophy and remodeling in a mouse model of transverse aorta constriction (TAC). This study was designed to determine the regulation of atorvastatin on cardiac autophagy and its association with the development of cardiac hypertrophy and dysfunction in the mice TAC model. Methods and results: TAC or sham operations were performed in male C57/L6 mice at 8 weeks of age. Atorvastatin (50 mg/kg/day) or vehicle (normal saline) were administered daily by oral gavage to TAC mice (n=10 per group). Echocardiography and real-time PCR data showed that chronic atorvastatin treatment for four weeks significantly attenuated pressure overload-induced cardiac hypertrophy and dysfunction, as well as cardiac mRNA level of atrial natriuretic factor (ANF), a biomarker of cardiac hypertrophy and heart failure. After 4 weeks of TAC, results from electron microscopy and Western blot showed that cardiac autophagy was activated, evidenced by the increased expression of microtubule-associated protein-1 light chain 3-II (LC3-II), Beclin-1, caspase-3, and the formation of autophagosomes. Interestingly, cardiac autophagy was further increased by the treatment of atorvastatin for 4 weeks. Western blot analysis showed phosphorylated Akt and mammalian target of rapamycin (p-mTor) decreased in the heart of TAC versus sham mice, which were further decreased by atorvastatin treatment. Conclusions: These findings suggest that atorvastatin attenuates cardiac hypertrophy and dysfunction in TAC mice probably through its regulation on cardiac autophagy via Akt/mTor pathways.

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